Diagnostic Workup of Upper-Limb Stress Fractures and ... · Diagnostic Workup of Upper-Limb Stress...

Diagnostic Workup of Upper-Limb StressFractures and Proximal Sesamoid Bone StressRemodeling

Susan M. Stover, DVM, PhD, Diplomate ACVS

Stress fractures and stress remodeling occur in specific locations within the scapula, humerus, andproximal sesamoid bones of racehorses. Knowledge of locations and of racehorse characteristics thatplace racehorses at high risk for scapular and humeral stress fractures and remodeling injuriesenhances veterinarians’ ability to detect scapular and humeral stress lesions. Detection of stressremodeling in proximal sesamoid bones is more challenging because of the small size and location ofthe lesions. Author’s address: JD Wheat Veterinary Orthopedic Research Laboratory, Departmentof VM:APC, School of Veterinary Medicine, University of California at Davis, One Shields Avenue,Davis, CA 95616; e-mail: [email protected]. © 2013 AAEP.

1. Introduction

As elite athletes, racehorses are susceptible to over-use injuries from repetitive motions incurred duringintense training and competition. Thoroughbredand Quarter Horse racehorses competing over flatracecourses have respective sets of occupationalskeletal injuries related to sites of concentrated highstresses incurred during task-specific training andracing activities. These injuries are typically re-ferred to as stress fractures or fatigue fractureswhen the affected site is associated with the cortexof a long bone and as stress remodeling when theaffected site is in a trabecular or subchondral loca-tion. The etiopathogenesis and biological repairmechanisms of these repetitive, overuse injuries aresimilar, irrespective of location. Fundamentally,injured bone tissue is capable of healing and regen-eration. However, continued training and racing ofhorses with stress fractures or sites of active stressremodeling can promote severe or catastrophic frac-

tures or irreversible osteoarthrosis when the under-lying bone tissue is weakened and can no longersupport the overlying articular cartilage.1,2 Thus,it is important to identify stress fractures and sitesof stress remodeling in racehorses so that affectedracehorses can be appropriately rehabilitated to al-low healing and return to athletic performance.

The purpose of this presentation is to enhanceawareness of preferential sites and features of stressfractures in the shoulder and arm of the forelimband of stress remodeling in the proximal sesamoidbones so that lesions in these regions are more likelyto be detected and appropriately managed to achieveresolution in racehorses.

2. Unsoundness Associated With a Stress Fracture orStress Remodeling

Lameness varies markedly in severity between af-fected horses, from unapparent or only a changein demeanor to non–weight-bearing.3,4 Lameness

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IN-DEPTH: RACING-RELATED LAMENESS

NOTES

is most commonly noted immediately after a train-ing or racing event3,4 and may appear to resolvewithin days of onset. Stress fractures and stressremodeling commonly affect bilateral limbs becausethe repetitive stresses associated with training andracing are incurred by both forelimbs or hindlimbs.5,6 Consequently, affected horses may notdemonstrate a distinct unilateral limb lameness.Instead, bilateral limb lameness may manifest as anunwillingness to perform at an expected level, achange in attitude, or unusual resistive behavior(for example, unwillingness to enter the startinggate). Poorly performing horses should be givena thorough physical examination to rule out non-musculoskeletal causes and elucidate skeletal inju-ries. Knowledge of the sites predisposed to stressfracture enhances ability to detect these injuries inracehorses.

3. Scapular Stress Fractures

Complete scapular fractures occur through the siteof a pre-existing stress fracture.2,5 Complete scap-ular fractures are the cause of 2% and 4% to 8%of fatal musculoskeletal injuries in Thoroughbredand Quarter Horse racehorses, respectively.2,7–9

Approximately 1 in 2500 Thoroughbred starters and1 in 1000 Quarter Horse starters incurs a completescapular fracture during a race.10 Although theoverall prevalence and incidence of scapular stressfractures in racehorses are unknown, scapular le-sions comprised 2% of positive findings for forelimbscintigraphic examinations in Thoroughbred race-horses, with some horses affected bilaterally.11

Scapular stress fractures occur along the typicalsite and configuration of complete scapular fracturesin racehorses (Fig. 1). Complete fractures occurtransversely or obliquely at the distal end of thespine of the scapula, dividing the scapula into alarge proximal component and a smaller distal com-ponent.5,7,12 Although comminution, distal propa-gation into the glenoid, and proximal propagation ofincomplete fracture lines are common, these are sec-ondary to the transverse/oblique fracture compo-nent. Stress fractures occur predominantly at thedistal end of the spine of the scapula in racehorsesthat died because of a complete scapular fracture,5,7

but stress fractures have also been reported to occurin the infraspinous fossa and supraspinous fossa,sites along the course of the transverse/oblique com-ponent of the complete fracture.4,5,13

Horses are at highest risk for complete scapularfracture early in their career (2 years of age) or as5-year-old or older horses, although racehorses ofall ages can be affected.4,10,13 They occur morecommonly in males than females. The right fore-limb is affected over twice as frequently as the leftforelimb, and bilateral complete fractures affect ap-proximately 9% of horses that died because of acomplete scapular fracture.10

Complete scapular fractures occur during racingor during training. Approximately a quarter of af-

fected Quarter Horses and a third of Thoroughbredshad never raced. Only half of unraced horses hadcompleted an official timed work. Horses that in-curred complete scapular fracture had fewer high-speed official timed works and races, loweraccumulated high-speed distance, and fewer days inactive training than age matched control horses.14

Consequently, racehorses that are in early high-speed training but behind that of their training co-hort, Quarter Horses that had a prolonged lay-up,and Thoroughbreds in high-speed training for alonger duration than that of their training cohortshould be examined for signs of scapular stressremodeling.14

Clinical Presentation and DetectionHorses affected with a scapular stress fracture areusually presented because of acute onset of lame-ness after a race or high-speed work.4,13 Lamenessis generally rated 2 to 3 of 5 (American Associationof Equine Practitioners lameness scale). Impor-tantly, the lameness may appear to resolve quickly.As expected, the lameness does not improve withdiagnostic and regional nerve blocks administeredat the level of the carpus and distally, althoughdiagnostic blocks should be done with caution be-cause of the risk of catastrophic fracture.

Physical examination is useful in detecting someaffected horses. Some horses have responded pos-itively to forelimb abduction and to palpation of thescapular spine (Fig. 2).4,13 Ultrasound examina-tion can be useful for detecting irregular periostealmodeling/remodeling, a stair-step in the spine or

Fig. 1. Bilateral scapulae from a racehorse that had a unilateral(right) complete fracture of the right scapula. Periosteal callusassociated with underlying bone resorption is present bilaterally,at the distal end of the neck of the scapulae. Periosteal callusattempts to buttress the spines, which are affected with an un-derlying intracortical weakness created by intracortical porosi-ties and low bone mineral density. The focal region ofosteoporosis creates a stress riser that facilitates bone fracture atotherwise physiologic loads. Stress remodeling occurs bilater-ally, but the weakest scapula fails catastrophically. In someaffected racehorses, both scapula catastrophically fracture.

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cortical surface, or hematoma,4,13 but these findingsmay not be present in horses with acute sub-perios-teal bone trauma (Fig. 3). Radiography has notbeen useful for detection of scapular stress frac-tures, largely because of limitations related to ex-tensive overlying soft tissues and bony structures ofthe thorax and neck. Scintigraphy remains thegold standard for detection of a focus of high meta-

bolic activity at sites consistent with scapular stressfracture and is useful in acute and chronic stages ofdisease (Fig. 4).4,11,13

RehabilitationConservative therapy of horses with scapular stressfracture has allowed return of racehorses to success-ful race performance, even after recurrence of ascapular stress fracture.4,13 Two months (60 days)of stall confinement, followed by 30 to 60 days ofturnout in a small paddock, has been recommendedbefore re-introduction to race training.4 Responseto treatment and length of rehabilitation is guidedby follow-up scintigraphic examination. Rehabili-tated horses have raced from 6 to 17 months (me-dian, 9 months) after diagnosis of a scapular stressfracture.13

4. Humeral Stress Fractures

Humeral injuries comprised 6% of lesions for Thor-oughbred racehorses examined scintigraphicallyfor a musculoskeletal problem15 and 10% of positivefindings for forelimb scintigraphic examinationsin Thoroughbred racehorses,11 with 15% to 29% ofhorses affected bilaterally.11,15 More recently, 20%of racehorses that had a bone scan that included thehumerus had a humeral lesion.16

Three-year-old racehorses are most commonly af-fected with humeral stress fracture; however, only32% to 51% of horses had some race experiencebefore diagnosis.3,15,17 Collectively, several studiessupport a left limb predilection for stress fracturesin live racehorses3,15,16 (although this predilectioncan vary with racetrack surface material16) and cat-astrophic fractures in deceased racehorses16; butboth forelimbs can be affected and a large proportionof affected racehorses have bilateral lesions.16

Fig. 2. The distal end of the spine of the scapula (right hand) canbe palpated between the supraspinatus muscle (cranially) andthe infraspinatus muscle (caudally) proximal to the groove be-tween the cranial and caudal parts of the greater tuberosity of thehumerus (left thumb).

Fig. 3. Transverse ultrasound images of the distal end of thespine of the left (asymptomatic) and right (affected) scapulae of aracehorse with a stress fracture of the right scapula. The spineof the left scapula is narrow and symmetric and has a normaldistinct, smooth surface contour. The spine of the right scapulais markedly thickened and has an abnormal irregular surfacecontour that is consistent with production of periosteal callus.

Fig. 4. Bone scan of the left scapula of a horse with a stressfracture at the distal end of the spine of the scapula.



Complete humeral fractures were the cause of 3%to 9% and 0% to 13% of fatal musculoskeletal inju-ries in Thoroughbred and Quarter Horse racehorses,respectively.2,7–9,18 Complete humeral fractures areknown to be associated with a pre-existing stressfracture (Fig. 5).6,7 Humeral stress fractures occurat several typical sites on the humerus in race-horses.3,6,15,16,19 Because stress fractures at caudo-proximal (37% of stress fractures), medialdiaphyseal (5%), and craniodistal (31%) sites occuralong the typical long oblique catastrophic completehumeral fracture that occurs in racehorses (Fig.6),6,7,16,20 the consequences of continuing to trainand race on stress fractures at these sites may bemore severe than stress remodeling at other sites.Most complete fractures (69–85%) from conveniencesamples of completely fractured humeri from race-horses extended through a caudoproximal region ofstress remodeling.6,16

Complete humeral fractures occur more com-monly during training (89–91%) and often at a slowgallop but also occur during racing.6,17 However,49% to 63% of affected horses had not raced beforediagnosis of a humeral stress fracture.6,15 Risk forcomplete humeral fracture is highest after an in-crease in exercise after a 2-month or longer layup.17

Clinical Presentation and DetectionHorses affected with a humeral stress fracture areusually presented because of acute onset of lame-

ness after a race or high-speed work but may have achronic insidious lameness duration of weeks tomonths.3,15 Lameness can range from 1 to 5 of 5(American Association of Equine Practitioners lame-ness scale), with most horses having grade 2 to 4lameness and some horses initially non–weight-bearing.3,15 Importantly, the lameness may appearto improve quickly, even within 24 hours.15 As ex-pected, the lameness does not improve with diagnos-tic and regional nerve blocks administered at thelevel of the carpus and distally,15 although diagnos-tic blocks should be done with caution because of therisk of catastrophic fracture. Lameness was exac-erbated in about half of affected horses after manip-ulation of the shoulder and elbow joints duringflexion, adduction, and abduction of the upper por-tion of the limb.3,15 Horses with severe lamenesstypically had a shortened cranial phase of the strideat the walk and trot.15

Radiographs have been useful for detection of hu-meral stress fractures but cannot be relied on fordiagnosis of acute stress fractures when bonechanges are insufficient to alter the radiographicappearance of affected humeri.3,15 Radiographicevidence of a stress fracture was observed in 56% to92% of affected horses, 69% to 80% of caudoproximalstress fractures, and 71% to 100% of craniodistalstress fractures (Fig. 7).3,15 In some cases, radio-graphic detection may have been enhanced becauseradiography was preceded by scintigraphic diagno-sis. It is notable that radiographic findings can benegative when lameness is first noticed but positive10 days to 12 months later.3

The author is unaware of any reports that dem-onstrated the diagnosis of humeral stress fracturesthrough the use of ultrasound examination. How-ever, ultrasound detection of periosteal new bonemay be achievable with knowledge of high-riskhorses and sites of predisposition.

Fig. 5. The proximal aspect of the left humeri from two differenthorses demonstrates a complete fracture coursing through anacute stress fracture (left) and a chronic stress fracture(right). The humerus on the left has periosteal callus that is athin (�2 mm thick) layer of highly vascular (red), rough-surfaced,woven bone. These features are characteristic of an acute peri-osteal reaction. The humerus on the right has a larger diameterperiosteal callus with two features. A thick (�8 mm in height),dense, central callus is indicative of bone that was formed andremodeled to yield more compact dense bone, which is moretypical of lamellar bone. Surrounding the central callus is a thinlayer of rough surfaced woven bone. Together, these two fea-tures indicate a recent exacerbation of a more chronic lesion.

Fig. 6. Lateral, medial, cranial, and caudal views of the lefthumerus illustrate the most common locations of stress fracturesin the humerus: caudoproximal at the neck of the humerus(red), craniodistomedial (blue), and medial (green).



Scintigraphy remains the gold standard for detec-tion of a focus of high metabolic activity at sitesconsistent with humeral stress fracture and is use-ful in acute and chronic stages of disease (Fig.8).4,11,13 In two separate studies, none of the horsesdiagnosed with a humeral stress fracture developeda catastrophic complete humeral fracture in the af-fected humerus.15,16 In contrast, none of the 32

racehorses that developed catastrophic fracture hada known record of a scintigraphic examination.16

RehabilitationConservative therapy of horses with humeral stressfracture has allowed resolution of lesions and adap-tation of the humerus to the stresses of racing byexpansion of the affected cortex (Fig. 9). Race-horses return to race performance, even on the oc-casion when a humeral stress fracture recurs and ismanaged in the same or another location.3,15 Ex-ercise restriction in the form of 4 weeks of stall restwith limited hand-walking if not lame at the walk;when not lame at the trot, 4 weeks of turnout in asmall area, then 4 to 8 weeks of turnout in pasture;and resumption of training.15 These periods wouldbe extended if lameness persisted at any stage.When possible, response to treatment and length ofrehabilitation is guided by follow-up scintigraphicexamination. Median time to return to racing afterstress fracture diagnosis was 7.5 months (range,5–22 months) for the 77% of horses that raced afterfracture.15 Median number of races after fracturewas 8.5 races (range, 1–33 races).15 No significantdifference was found for mean earnings per startbetween before and after fracture.15 However, hu-meral stress fractures can recur at the same or dis-tant sites in the same or contralateral limbs.3,15

5. Proximal Sesamoid Bone Stress Remodeling

Proximal sesamoid bone fracture (with or withoutassociated metacarpal bone fracture) is the mostfrequent catastrophic (fatal) musculoskeletal injuryin racehorses, accounting for 45% to 50% of Thor-oughbred injuries and 37% to 40% of Quarter Horseinjuries.1,2,8,18 Although small displaced abaxial,apical, and basilar fragments are common in race-horses, these findings do not lead to catastrophicfractures of the proximal sesamoid bones. Com-plete transverse or oblique fractures of the proximalsesamoid bones disrupt transmission of force fromthe suspensory ligament to the distal sesamoidean

Fig. 7. Lateromedial radiograph of the left elbow of a racehorsedemonstrating periosteal callus (arrows), consistent with stressfracture of the craniodistomedial aspect of the humerus.

Fig. 8. Lateral view bone scans of humeri demonstrating cra-nioproximal (upper left), caudoproximal (upper center), deltoidtuberosity (upper right), craniodistal (lower left), middle diaphy-seal (lower center), and caudodistal (lower right) lesions.

Fig. 9. Lateromedial radiographs of the proximal aspect of thehumerus from the same horse at the initiation of clinical signs(left) 1 month later (center) and 3 months later (right). Thecontour of the humeral neck changes from the normal concavecontour to convex with apposition of periosteal callus to bluntedwith remodeling and flattening of the callus to result in boneadaptation by residual expansion (thickening) of the cortex.



ligaments and are the most common cause of fetlockinjuries that are catastrophic because they disruptthe integrity of the suspensory apparatus.21

The most common configuration for catastrophicfetlock injury is biaxial proximal sesamoid bonefracture.2,9,21 Complete, transverse, articular frac-ture that separates the body from the base of themedial proximal sesamoid bone is accompanied bycomplete, oblique or transverse, articular fracture ofthe lateral proximal sesamoid bone (Fig. 10).21

Fractures often have some comminution and disrup-tion of adjacent soft tissues. Although other prox-imal sesamoid bone fracture configurations alsodisrupt the suspensory apparatus, the focus of thisreport will be on medial proximal sesamoid bonefracture because of lesions that probably predisposeto fracture and initiation of suspensory apparatusfailure.22,23

Two lesions probably predispose to medial proxi-mal sesamoid bone fracture.22,23 Both lesions arefoci of bone resorption that occur in response to thelocal accumulation of microdamage acquired fromthe repetitive load cycles associated with trainingand racing. The first lesion that was recognizedoccurs on the palmar margin of the proximal sesa-moid bone (Fig. 11).22 The second lesion ismore common and occurs consistently within a sub-chondral, abaxial location within the medial proxi-mal sesamoid bone (Fig. 12).23 Both lesions arelarge enough to create a stress riser sufficientlylarge to initiate bone fracture but small enough,and, in difficult locations, to detect with the use ofradiography.

Clinical Presentation and DetectionThe clinical signs that distinguish horses with im-pending catastrophic fracture of the proximal sesa-moid bones from horses that can race successfullywithout injury is challenging. However, severalpieces of evidence demonstrate that some features ofhorse signalment and history and some clinicalsigns are associated with increased risk for cata-strophic fracture.

Racehorses that have catastrophic failure of thefetlock suspensory apparatus, including horses withproximal sesamoid bone fractures, are typicallyolder horses (�5 years old), more likely to be malethan female, have had a long racing career (�20

Fig. 10. Dorsopalmar radiograph of proximal sesamoid bonespecimens illustrates a common fracture configuration. The me-dial proximal sesamoid bone incurs a relatively simple transversefracture that splits a larger proximal fragment from thebase. The lateral proximal sesamoid bone fracture varies morebut commonly has an oblique fracture that separates the apexfrom the body.

Fig. 11. Dorsal (articular) surface of the proximal sesamoid bones from the fractured leg of a racehorse with fractures of the medialand lateral proximal sesamoid bones. The fracture surfaces of the medial proximal sesamoid bone have been opened to visualize thestress-remodeling lesion (ellipses) on the palmar aspect of the bone.



races), and have experienced prolonged high exer-cise intensity.24,25 Furthermore, horses that had acatastrophic fetlock injury were 3 times more likelyto have had a palpable abnormality of the suspen-sory ligament; they were 2 times more likely to havehad an abnormality of the fetlock joint on pre-raceinspection; and the pre-race veterinary inspectorwas 8 to 14 times more likely to have considered thehorse to be at higher risk.9,24 The usefulness ofthese findings is tempered by the low specificity ofthe findings; that is, a much larger number of horseshad a similar abnormality but did not receive asubsequent injury in the associated race.26 How-ever, when the long-term performance of horses isconsidered, 45% of horses with signs of mild suspen-sory apparatus injury had a training remissioncaused by a severe musculoskeletal injury within 3months compared with 14% of horses without thesame signs.27 Thus, horses with mild injuries tothe suspensory apparatus are much more likely todrop out of the racing pool.

The palmar and subchondral locations of the fociof stress remodeling create challenges in lesion de-tection. Synovial effusion and synovial fluid abnor-malities are unlikely to result directly from stress-remodeling lesions in the proximal sesamoid bonesbecause neither lesion is intra-articular or intra-thecal. However, synovial effusion of the fetlockjoint may be present because other degenerativelesions (eg, proximodorsal proximal phalangealosteochondral fragments, score lines, palmar osteo-chondral disease) usually accompany proximalsesamoid bone lesions. Similarly, intra-synovialanesthesia may not result in improvements in lame-

ness unless lameness is caused by other attendantintra-synovial degenerative changes. However, re-gional anesthesia that desensitizes the fetlock re-gion is likely to improve any observed lameness orresult in enhancing lameness in the contralaterallimb because stress remodeling is often bilateral.

Radiographs have not been useful for detection oflesions that might predispose to catastrophic frac-ture of the proximal sesamoid bone.21 Paradoxi-cally, among all proximal sesamoid bones fromhorses that had a catastrophic proximal sesamoidbone fracture, the likelihood of bone fracture wasreduced by half when the bone had radiographicevidence of osteophytes and to less than a quarterwhen the bone had prominent vascular channels.21

The two sites of stress remodeling are in difficultlocations to visualize radiographically because ofoverlying bone tissue and contours (Fig. 13).Whereas the abaxial site appears to be associatedwith abaxial vascular channels, the subchondralsite appears to be associated with basilar vascularchannels.

Radiographs are useful for detecting other lesionsof the fetlock that usually (but not always) accom-pany proximal sesamoid bone disease. Horses thatsustained catastrophic fracture of the proximal ses-amoid bones often have degenerative lesions of themetacarpal condyle (palmar osteochondral disease),osteochondral degeneration or fragmentation of thedorsoproximal margin of the proximal phalanx, andother articular cartilage degenerative changes.However, it is not known how often these changesare present without proximal sesamoid bone disease.

Fig. 12. Dorsal (articular) surface of the proximal sesamoid bones from the fractured leg of a racehorse with fractures of the medialand lateral proximal sesamoid bones. The fracture surfaces of the medial proximal sesamoid bone have been opened to visualize thestress-remodeling lesion (circles) in an abaxial subchondral location.



Ultrasound examination might be useful for de-tecting abnormal bone contours on the palmaraspect of the proximal sesamoid bone. Unfortu-nately, this region of the bone is normally irregularin contour; therefore, distinction of contours causedby lesions from normal contours could be difficult.The author is unaware of any reports that demon-strated the diagnosis of proximal sesamoid bonestress remodeling through the use of ultrasoundexamination.

Magnetic resonance imaging has potential for de-tection of stress-remodeling lesions. Technologyand image acquisition and analysis softwareenhancements for standing magnetic resonanceimaging machines may make detection of stress-remodeling lesions in the proximal sesamoid bonefeasible in horses without the risks associated withgeneral anesthesia.

Clinical computed tomography currently requiresgeneral anesthesia, and, in our experience, the smallfoci of stress remodeling in the proximal sesamoidbones makes lesion detection challenging. En-hancements in computed tomography technologycould increase chances of lesion detection.

Scintigraphy remains the gold standard for detec-tion of a focus of high metabolic activity at sitesconsistent with stress remodeling (Fig. 14). Thechallenge is differentiating changes associated withadaptive remodeling of the proximal sesamoid bonein response to the increased loads associated withtraining and racing22,28 from pathologic or maladap-tive remodeling. Furthermore, it can be difficultto differentiate increased activity in the palmaraspect of the metacarpal condyle from increased ac-tivity in the proximal sesamoid bone, particularlybecause palmar osteochondral disease often accom-panies subchondral proximal sesamoid bone le-sions.23 Because flexion of the fetlock moves theproximal sesamoid bones proximal to the metacar-pal condyle, a lateral image of the flexed fetlock mayallow differentiation of proximal sesamoid activityfrom metacarpal condylar activity.

Rehabilitation

Bone lesions are capable of healing. Affectedhorses need time without intensive training andracing to allow resolution of bone lesions. Clini-cally, the difficulty is detecting lesions so that heal-ing progression can be monitored to guiderehabilitation of affected horses.

Acknowledgment

This work was supported by the California HorseRacing Board Racing Safety Program.

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Fig. 14. Bilateral distal forelimb bone scan illustrating in-creased radiopharmaceutical uptake in a region consistent with alesion in the medial proximal sesamoid bone.

Fig. 13. Palmar (red arrows) and subchondral abaxial (black arrows) sites of stress remodeling (red filled regions) in the medialproximal sesamoid bone, superimposed on medial (left), transverse section (middle), and palmar (right) views of the fetlock region.



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